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Distribution and Function of Filamentous and Globular Actin in Mitochondrial Translocation During Ascidian Sperm Activation

Published online by Cambridge University Press:  02 July 2020

E. Zebadua
Affiliation:
Sperm Cell Biology and Gamete Ultrastructure Laboratory, Department of Biological Science, California State University, Fullerton, 92834-6850.
L. Blackwell
Affiliation:
Sperm Cell Biology and Gamete Ultrastructure Laboratory, Department of Biological Science, California State University, Fullerton, 92834-6850.
R.A. Koch
Affiliation:
Sperm Cell Biology and Gamete Ultrastructure Laboratory, Department of Biological Science, California State University, Fullerton, 92834-6850.
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Abstract

During fertilization in the sea squirt, Ascidia ceratodes,the penetration process of requires mitochondrial translocation, a process that defines sperm activation in this species, to generate the driving force for passage through the vitelline coat. When a sperm cell come into contact with an egg, the mitochondrion translocates off the head and migrates along the tail via an actimmyosin-dependent process. The presence of actin and myosin on the head and tail has been demonstrated. However, the nature of the relative distribution of filamentous actin (F-actin) and monomeric actin (G-actin) has not been thoroughly studied. And, whereas the signaling cascade that leads to myosin activation has been studied, the events leading to actin polymerization and whether it is required for mitochondrial translocation has not.

This project addresses two research questions: What is the distribution of F-actin and G-actin in unactivated and activated sperm cells? And, can preexisting F-actin support mitochondrial translocation or must actin polymerization occur simultaneously with the mitochondrial translocation process?

Type
Student Research Forum (Organized by R. Koch and Z. Mason)
Copyright
Copyright © Microscopy Society of America 2001

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References

1 Lambert, C.C.. Dev. Biol. 116(1986)168.CrossRefGoogle Scholar

2 Butler, D. et al. Dev. Biol. 215(1999)453.CrossRefGoogle Scholar

3 Supported by NIH R25-GM56820 and R15HD36500.Google Scholar